The products of protooncogenes are now widely recognized to play pivotal roles in growth stimulatory pathways and in differentiation. The products of the tumor suppressor genes are now known to exert negative effects on cell proliferation and evidence exists for involvement of these gene products in the pathway for diffusible negative factors. There is overwhelming evidence that changes in the dominant oncogenes and recessive tumor suppressor genes have great importance in the genesis of common human cancers. Major recent advances in growth control include (i) cloning of two new tumor suppressor genes, the Wilm's tumor gene and the type I neurofibromatosis gene; (ii) the characterization of the kit ligand, a novel hematopoietic growth factor, (iii) the description of a new family of hematopoietic receptors and their oncogenic activation; (iv) the description of ras-related gene products, including one encoded by a tumor suppressor gene, that suppress stimulatory signals; (v) the identification tyrosine kinase substrates that function as second messengers; (vi) examples of linkage between cell surface receptors with no previously known signal transduction capability and cytoplasmic tyrosine kinases; (vii) the demonstration that nuclear protooncogene products directly regulate gene transcription and that other known transcriptional regulators can contribute to neoplastic transformation; (viii) definition of roles for cell cycle kinases in growth regulation; (ix) implication of the retinoblastoma tumor susceptibility gene product in the pathway for transcriptional suppression of the protooncogene, c-myc; and (x) demonstration that p53 functions to suppress cell proliferation and that mutations and deletions of p53 gene are common occurrences in human and experimental malignancies. The concurrent meetings on "Positive Growth Control" and "Negative Growth Control" will address these and other major discoveries and approach important cur-rent problems including the interplays between positive and negative growth regulatory pathways. There will be three joint plenary sessions involving participants of both meetings and covering topics of common interest including the cell cycle, ras-related proteins and regulation of transcription. There will be an additional eight plenary sessions in each of the two meetings covering a wide range of topics pertinent to growth regulation and cancer development and progression. Poster sessions will cover topics similar to those addressed in plenary sessions. Meetings on the important and rapidly moving fields of positive and negative growth control are appropriate and timely. Having concurrent meetings on these topics should provide significant synergy and beneficial interactions that otherwise could not be achieved.